We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Atypical ductal hyperplasia: update on diagnosis, management, and molecular landscape.
- Authors
Kader, Tanjina; Hill, Prue; Rakha, Emad A.; Campbell, Ian G.; Gorringe, Kylie L.
- Abstract
<bold>Background: </bold>Atypical ductal hyperplasia (ADH) is a common diagnosis in the mammographic era and a significant clinical problem with wide variation in diagnosis and treatment. After a diagnosis of ADH on biopsy a proportion are upgraded to carcinoma upon excision; however, the remainder of patients are overtreated. While ADH is considered a non-obligate precursor of invasive carcinoma, the molecular taxonomy remains unknown.<bold>Main Text: </bold>Although a few studies have revealed some of the key genomic characteristics of ADH, a clear understanding of the molecular changes associated with breast cancer progression has been limited by inadequately powered studies and low resolution methodology. Complicating factors such as family history, and whether the ADH present in a biopsy is an isolated lesion or part of a greater neoplastic process beyond the limited biopsy material, make accurate interpretation of genomic features and their impact on progression to malignancy a challenging task. This article will review the definitions and variable management of the patients diagnosed with ADH as well as the current knowledge of the molecular landscape of ADH and its clonal relationship with ductal carcinoma in situ and invasive carcinoma.<bold>Conclusions: </bold>Molecular data of ADH remain sparse. Large prospective cohorts of pure ADH with clinical follow-up need to be evaluated at DNA, RNA, and protein levels in order to develop biomarkers of progression to carcinoma to guide management decisions.
- Subjects
HYPERPLASIA; BREAST tumors; DUCTAL carcinoma; CANCER invasiveness; BREAST cancer; MEDICAL care
- Publication
Breast Cancer Research, 2018, Vol 20, Issue 1, pN.PAG
- ISSN
1465-5411
- Publication type
journal article
- DOI
10.1186/s13058-018-0967-1